Despite being the most common movement disorder, ET remains a pathophysiological enigma. The proposed pathogenesis of ET has been attributed to abnormal discharges through multiple pathways including the cerebellothalamocortical pathway and the Guillain-Mollaret triangle. The cerebellothalamocortical network describes the relationship between the inferior olive, cerebellum, red nucleus, thalamus, and cortex, while the Guillain-Mollaret Triangle is comprised of connections between the red nucleus, inferior olivary nucleus, and contralateral dentate nucleus.

We report two cases of spontaneous resolution of ET following acute ischemic stroke.

The first patient’s MRI showed a small infarct in the right frontal lobe in the prefrontal gyrus extending into the centrum semiovale. This lesion ameliorated his contralateral ET, and the changes persisted through his one-year follow-up. We speculate that his infarct interrupted the cortical input to the cerebellothalamocortical network. The second patient’s MRI demonstrated a small left lateral medullary infarct, which clinically resulted in temporary resolution of bilateral upper extremity ET. It is hypothesized that the clinical improvement in tremor was due to interruption of inferior olivary nucleus input to the Guillain-Mollaret Triangle. This patient’s ET returned 1 month after his infarct, likely due to recovery from an incomplete lesion within the tremor circuit.  

Our cases add to the growing body of radiographic evidence of “curative strokes” wherein lesions within the cerebellothalamocortical network and Guillain-Mollaret Triangle cause resolution of ET. The radiographic data presented in our cases, alongside data gleaned from a multidisciplinary approach including neurophysiologic studies, neuropathology, and neurosurgery allow for a better understanding of the neuro-circuitry affecting ET.